Browsing Pathways

The molecular mechanisms of glucose-dependent insulinotropic peptide (GIP) involve its role as an incretin hormone that stimulates insulin secretion in response to nutrients, particularly fats and carbohydrates, in the small intestine. GIP is produced by endocrine K cells in the small intestine lining and acts on GIP receptors found in various organs, including the brain, bone, and fat tissue. When GIP is released, it stimulates the release of insulin, which helps regulate blood sugar levels and promote glucose uptake into cells for energy. GIP also slows down the rate at which food passes through the small intestine, which helps to increase the absorption of nutrients. In the brain, GIP stimulates the growth of cells that can divide and eventually form new cells. In bone, GIP increases the formation of bone while decreasing bone breakdown. In fat tissue, GIP is known to increase the amount of fat in the body by increasing the production of fat cells and promoting the storage of fat. GIP plays a role in controlling blood sugar levels by stimulating the release of insulin. Insulin is a hormone produced by the pancreas that helps regulate blood sugar levels by promoting glucose uptake into cells. When GIP is released in response to the presence of nutrients in the small intestine, it stimulates insulin release, which helps lower blood sugar levels. This process is vital for maintaining normal blood sugar levels and overall health. Abnormal blood sugar levels can have serious health consequences. High blood sugar levels (hyperglycemia) can lead to diabetes, which can cause various severe health problems, including heart disease, nerve damage, blindness, and kidney disease. Low blood sugar levels (hypoglycemia) can also be harmful, causing symptoms such as dizziness, sweating, and difficulty concentrating.

The RAS-ERK and PI3K-mTOR signaling pathways

Schematic representation of the CNS-immune system crosstalk. There are bi-directional circuits linking CNS and immune system. The CNS can communicate with the immune system to modulate its activity, through different ways: through the autonomic nervous system (via the sympathetic and vagus nerve innervation, see the text for deeper details), the catecholaminergic pathway, or the neuropeptides and hormones release. In this context, leptin modulates immune system, by increasing the activation of T cells and decreasing Treg cells functions, thus representing a key player in the susceptibility to immune-mediated disorders (β2R, β2 receptor; α7 nAChR, α7 subunit of the nicotinic acetylcholine receptor)

Certainly! When elastic fibers undergo fragmentation, it often occurs in the context of tissue damage or remodeling. This damage can trigger a cellular response that includes the release of small membrane-bound particles called matrix vesicles. Matrix vesicles are secretory vesicles originating from various cell types, including osteoblasts, chondrocytes, and vascular smooth muscle cells. These matrix vesicles play a crucial role in the initiation of mineralization processes in tissues. Within the matrix vesicles, there is a concentration of calcium and phosphate ions, which are essential components for the formation of hydroxyapatite crystals, the primary mineral found in bone and ectopic calcifications. Once released into the extracellular matrix, these matrix vesicles can serve as nucleation sites for the deposition of calcium phosphate crystals. The presence of high concentrations of calcium and phosphate ions within the matrix vesicles promotes the formation of mineral nuclei, which subsequently grow and aggregate to form larger crystalline structures. This process of nucleation and crystal growth is the initial step in the formation of calcifications. Once the calcium phosphate crystals reach a critical size, they can further propagate and mineralize surrounding tissues, leading to the development of ectopic calcifications. Therefore, the fragmentation of elastic fibers can indirectly contribute to ectopic calcification by triggering the release of matrix vesicles containing calcium and phosphate ions. These vesicles serve as seed sites for the deposition of calcium phosphate crystals, initiating the calcification process and ultimately leading to the formation of mineralized deposits within tissues.